Kaiso (ZBTB33) Downregulation by Mirna-181a Inhibits Cell Proliferation, Invasion, and the Epithelial–Mesenchymal Transition in Glioma Cells

Background/Aims: Kaiso (ZBTB33) expression is closely associated with the progression of many cancers and microRNA (miRNA) processing. MiR-181a plays critical roles in multiple cancers; however, its precise mechanisms in glioma have not been well clarified. The goal of this study was to evaluate the interaction between Kaiso and miR-181a in glioma. Methods: Quantitative real-time PCR (qRT-PCR) was performed to detect the levels of Kaiso and miR-181a in glioma tissues and cell lines. Cell proliferation, invasion, and the epithelial–mesenchymal transition (EMT) were evaluated to analyze the biological functions of miR-181a and Kaiso in glioma cells. The mRNA and protein levels of Kaiso were measured by qRT-PCR and western blotting, respectively. Meanwhile, luciferase assays were performed to validate Kaiso as a miR-181a target in glioma cells. Results: We found that the level of miR-181a was the lowest among miR-181a–d in glioma tissues and cell lines, and the low level of miR-181a was closely associated with the increased expression of Kaiso in glioma tissues. Moreover, transfection of miR-181a significantly inhibited the proliferation, invasion, and EMT of glioma cells, whereas knockdown of miR-181a had the opposite effect. Bioinformatics analysis predicted that Kaiso was a potential target gene of miR-181a, and the luciferase reporter assay demonstrated that miR-181a could directly target Kaiso. In addition, Kaiso silencing had similar effects as miR-181a overexpression in glioma cells, whereas overexpression of Kaiso in glioma cells partially reversed the inhibitory effects of the miR-181a mimic. Conclusionss: miR-181a inhibited the proliferation, invasion, and EMT of glioma cells by directly targeting and downregulating Kaiso expression.

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MicroRNA-6884-5p Regulates the Proliferation, Invasion, and EMT of Gastric Cancer Cells by Directly Targeting S100A16

Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics ◽

10.3727/096504019x15753718797664 ◽

2020 ◽

Vol 28 (3) ◽

pp. 225-236 ◽

Cited By ~ 2

Author(s):

Huifang Lv ◽

Honglin Hou ◽

Huijun Lei ◽

Caiyun Nie ◽

Beibei Chen ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Lines ◽

Epithelial Mesenchymal Transition ◽

Close Association ◽

Luciferase Reporter ◽

Inhibitory Effects ◽

Gastric Cancer Cells ◽

Mesenchymal Transition ◽

Qrt Pcr ◽

Polymerase Chain

S100 binding protein A16 (S100A16) expression levels are closely associated with microRNA (miRNA) processing. Higher levels of S100A16 are reported during the progression of many cancers. Our study mainly explored the interaction between S100A16 and miR-6884-5p in gastric cancer (GC). Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the level of S100A16 and miR-6884-5p in GC tissues and cell lines. The si-S100A16, pcDNA-S100A16, miR-6884-5p mimic or inhibitor was transfected into GC cells, and the effects of S100A16 and miR-6884-5p on the proliferation, invasion, and epithelial‐mesenchymal transition (EMT) were explored by qRT-PCR and Western blot assays. Luciferase assays were performed to validate S100A16 as an miR-6884-5p target in GC cells. In our study, we found that the level of miR-6884-5p was significantly decreased and the expression of S100A16 was significantly increased in GC tissues and cell lines. There was a close association between these changes. Knockdown of S100A16 significantly inhibited the proliferation, invasion, and EMT of GC cells. The bioinformatics analysis predicted that S100A16 is a potential target gene of miR-6884-5p, and the luciferase reporter assay confirmed that miR-6884-5p could directly target S100A16. Introduction of miR-6884-5p to GC cells had similar effects to S100A16 silencing. Overexpression of S100A16 in GC cells partially reversed the inhibitory effects of the miR-6884-5p mimic. miR-6884-5p inhibited the proliferation, invasion, and EMT of GC cells by directly decreasing S100A16 expression.

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Long non-coding RNA FOXD2-AS1 promotes cell proliferation, metastasis and EMT in glioma by sponging miR-506-5p

Open Medicine ◽

10.1515/med-2020-0175 ◽

2020 ◽

Vol 15 (1) ◽

pp. 921-931

Author(s):

Juan Zhao ◽

Xue-Bin Zeng ◽

Hong-Yan Zhang ◽

Jie-Wei Xiang ◽

Yu-Song Liu

Keyword(s):

Cell Proliferation ◽

Epithelial Mesenchymal Transition ◽

Human Cancer ◽

Glioma Cells ◽

Suppressor Gene ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Mesenchymal Transition ◽

Non Coding Rna ◽

Long Non Coding Rna

AbstractLong non-coding RNA forkhead box D2 adjacent opposite strand RNA 1 (FOXD2-AS1) has emerged as a potential oncogene in several tumors. However, its biological function and potential regulatory mechanism in glioma have not been fully investigated to date. In the present study, RT-qPCR was conducted to detect the levels of FOXD2-AS1 and microRNA (miR)-506-5p, and western blot assays were performed to measure the expression of CDK2, cyclinE1, P21, matrix metalloproteinase (MMP)7, MMP9, N-cadherin, E-cadherin and vimentin in glioma cells. A luciferase reporter assay was performed to verify the direct targeting of miR-506-5p by FOXD2-AS1. Subsequently, cell viability was analyzed using the CCK-8 assay. Cell migration and invasion were analyzed using Transwell and wound healing assays, respectively. The results demonstrated that FOXD2-AS1 was significantly overexpressed in glioma cells, particularly in U251 cells. Knockdown of FOXD2-AS1 in glioma cells significantly inhibited cell proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) and regulated the expression of CDK2, cyclinE1, P21, MMP7 and MMP9. Next, a possible mechanism for these results was explored, and it was observed that FOXD2-AS1 binds to and negatively regulates miR-506-5p, which is known to be a tumor-suppressor gene in certain human cancer types. Furthermore, overexpression of miR-506-5p significantly inhibited cell proliferation, migration, invasion and EMT, and these effects could be reversed by transfecting FOXD2-AS1 into the cells. In conclusion, our data suggested that FOXD2-AS1 contributed to glioma proliferation, metastasis and EMT via competitively binding to miR-506-5p. FOXD2-AS1 may be a promising target for therapy in patients with glioma.

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Tumor-Suppressive Function of lncRNA-MEG3 in Glioma Cells by Regulating miR-6088/SMARCB1 Axis

BioMed Research International ◽

10.1155/2020/4309161 ◽

2020 ◽

Vol 2020 ◽

pp. 1-15 ◽

Cited By ~ 1

Author(s):

Xin Gong ◽

Meng-Yi Huang

Keyword(s):

Cell Proliferation ◽

Epithelial Mesenchymal Transition ◽

Glioma Cells ◽

Luciferase Reporter ◽

Favorable Effect ◽

Mesenchymal Transition ◽

Gene Assay ◽

And Migration ◽

Proliferation And Migration ◽

Glioma Progression

Objective. Mounting evidence has elaborated the implication of long noncoding RNAs (lncRNAs) in tumorigenesis of several cancers, including glioma. However, little was known about the mechanism of lncRNA maternally expressed gene 3 (MEG3) in the development and progression of glioma. This work is designed to explore the effect of MEG3 on glioma progression and its possible mechanism. Methods. Expressions of lncRNA-MEG3 and SMARCB1 were detected in human glioblastoma U87 and U251 cell lines. Gain and loss of function of MEG3 or/and miR-6088 was performed in U87 and U251 cells to observe its effect on cell proliferation and migration as well as on epithelial-mesenchymal transition (EMT) related markers. Luciferase reporter gene assay was employed to inspect the interactions among MEG3, miR-6088, and SMARCB1. Results. MEG3 and SMARCB1 expressions were downregulated in glioma cells. Transfection of pcDNA3.1-MEG3 or pcDNA3.1-SMARCB1 plasmids could clearly block cell proliferation, migration, and EMT progression. MEG3 functions as a sponge for miR-6088, while SMARCB1 is a downstream protein of miR-6088. Transfection of miR-6088 mimic or si-SMARCB1 could obviously reverse the favorable effect of pcDNA3.1-MEG3 on glioma progression. Conclusion. Collectively, the evidence in this study indicated that MEG3 was downregulated in glioma cells and inhibited proliferation and migration of glioma cells via regulating miR-6088/SMARCB1 axis.

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Long noncoding RNA XIST regulates the EGF receptor to promote TGF-β1-induced epithelial–mesenchymal transition in pancreatic cancer

Biochemistry and Cell Biology ◽

10.1139/bcb-2018-0274 ◽

2020 ◽

Vol 98 (2) ◽

pp. 267-276 ◽

Cited By ~ 1

Author(s):

Lei Zou ◽

Feng-Rong Chen ◽

Ren-Pin Xia ◽

Hua-Wei Wang ◽

Zhen-Rong Xie ◽

...

Keyword(s):

Pancreatic Cancer ◽

Cell Proliferation ◽

Growth Factor ◽

Epithelial Mesenchymal Transition ◽

Luciferase Reporter ◽

Mesenchymal Transition ◽

Clinical Specimens ◽

Qrt Pcr ◽

Reporter Assays ◽

Tgf Β1

Background: This study focuses on the lncRNA XIST (X inactive-specific transcript), an lncRNA involved in multiple human cancers, and investigates the functional significance of XIST and the molecular mechanisms underlying the epithelial–mesenchymal transition (EMT) in pancreatic cancer (PC). Methods: Clinical specimens from 25 patients as well as 5 human PC cell lines were analyzed for XIST, YAP, and microRNA(miR)-34a by quantitative real-time PCR (qRT-PCR) and immunohistochemistry. To investigate how XIST influences cell proliferation, invasiveness, and apoptosis in PC, we performed the CCK-8 assays, Transwell assays, and flow cytometry. Luciferase reporter assays, qRT-PCR, and Western blot were applied to prove that miR-34a directly binds to XIST. Results: Up-regulation of XIST and Yes associated protein (YAP) and down-regulation of miR-34a were consistently observed in the clinical specimens and PC cell lines. Silencing XIST reduced the expression of YAP and suppressed transforming growth factor (TGF)-β1-induced EMT, while over-expression of XIST increased the expression of YAP and promoted EMT. In addition, inhibition of epidermal growth factor receptor (EGFR) hampered the XIST-promoted EMT. The results from the luciferase reporter assays confirmed that miR-34a directly targets XIST and suggested that XIST regulates cell proliferation, invasiveness, and apoptosis in PC by sponging miR-34a. Conclusions: XIST promotes TGF-β1-induced EMT by regulating the miR-34a–YAP–EGFR axis in PC.

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miR-16 Inhibits Extracellular Signal-Regulated Kinases (ERK) Mitogen-Activated Protein Kinases (MAPK) Signaling to Affect Epithelial-Mesenchymal Transition (EMT) and Invasion of Glioma Cells

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2022.2945 ◽

2022 ◽

Vol 12 (4) ◽

pp. 848-853

Author(s):

Peng Sun ◽

Duojiao Fan ◽

Jing Cao ◽

Haiyan Zhou ◽

Fan Yang ◽

...

Keyword(s):

Cell Proliferation ◽

Glioma Cell ◽

Epithelial Mesenchymal Transition ◽

Glioma Cells ◽

Mapk Signaling ◽

Luciferase Assay ◽

Luciferase Reporter ◽

Mesenchymal Transition ◽

U251 Cells ◽

E Cadherin

Abnormal MEK1 expression is associated with tumor cell EMT, invasion and metastasis. Decreased miR-16 level is associated with glioma. Bioinformatics analysis showed a relationship between miR-16 and MEK1. This study assessed whether miR-16 regulates MEK1 expression and affects glioma cell EMT and invasion. The tumor tissues and adjacent glioma tissues were collected to measure miR-16 and MEK1 mRNA. The dual luciferase assay validated the relation of miR-16 with MEK1. U251 cells were cultured and assigned into NC group and mimic group, followed by analysis of cell biological behaviors, and MEK1, p-ERK1/2, E-cadherin, N-Cadherin expression. Compared with adjacent tissues, miR-16 expression was significantly decreased and MEK1 was elevated in glioma tissues. Compared with HEB, miR-16 in glioma U251 and SHG44 cells was decreased and MEK1 was increased. Dual luciferase reporter gene experiments confirmed the relation of miR-16 with MEK1. Transfection of miR-16 mimic significantly down-regulated MEK1, p-ERK1/2 and N-cadherin in U251 cells, upregulated E-cadherin, inhibited cell proliferation, promoted apoptosis, and attenuated EMT and invasion of glioma cells. In conclusion, decreased miR-16 expression and increased MEK1 expression is related to glioma pathogenesis. Overexpression of miR-16 can inhibit MEK1 expression, ERK/MAPK signaling, glioma cell proliferation, promote apoptosis, and attenuate EMT and invasion.

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microRNA-802 inhibits epithelial-mesenchymal transition through targeting flotillin-2 in human prostate cancer

Bioscience Reports ◽

10.1042/bsr20160521 ◽

2017 ◽

Vol 37 (2) ◽

Cited By ~ 14

Author(s):

Dawei Wang ◽

Guoliang Lu ◽

Yuan Shao ◽

Da Xu

Keyword(s):

Prostate Cancer ◽

Cell Proliferation ◽

Cell Lines ◽

Cell Apoptosis ◽

Epithelial Mesenchymal Transition ◽

Xenograft Model ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Mesenchymal Transition

miRNAs are a class of non-coding RNAs that exert critical roles in various biological processes. The aim of the present study was to identify the functional roles of miR-802 in regulating epithelial–mesenchymal transition (EMT) in prostate cancer (PCa). miR-802 expression was detected in 73 pairs of PCa samples and PCa cell lines (PC3 and DU145 cells) by qRT-PCR. Cell proliferation was detected using MTT assay, and cell apoptosis was evaluated using flow cytometry. Transwell assay was conducted to investigate cell migration and invasion. Expression analysis of a set of EMT markers was performed to explore whether miR-802 is involved in EMT program. Xenograft model was established to investigate the function of miR-802 in carcinogenesis in vivo. The direct regulation of Flotillin-2 (Flot2) by miR-802 was identified using luciferase reporter assay. miR-802 was remarkably down-regulated in PCa tissues and cell lines. Gain-of-function trails showed that miR-802 serves as an ‘oncosuppressor’ in PCa through inhibiting cell proliferation and promoting cell apoptosis in vitro. Overexpression of miR-802 significantly suppressed in vivo PCa tumor growth. Luciferase reporter analysis identified Flot2 as a direct target of miR-802 in PCa cells. Overexpressed miR-802 significantly suppressed EMT, migration and invasion in PCa cells by regulating Flot2. We identified miR-802 as a novel tumor suppressor in PCa progression and elucidated a novel mechanism of the miR-802/Flot2 axis in the regulation of EMT, which may be a potential therapeutic target.

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The Lncrna-TUG1/EZH2 Axis Promotes Pancreatic Cancer Cell Proliferation, Migration and EMT Phenotype Formation Through Sponging Mir-382

Cellular Physiology and Biochemistry ◽

10.1159/000479990 ◽

2017 ◽

Vol 42 (6) ◽

pp. 2145-2158 ◽

Cited By ~ 52

Author(s):

Liang Zhao ◽

Hongwei Sun ◽

Hongru Kong ◽

Zongjing Chen ◽

Bicheng Chen ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Lines ◽

Rna Binding ◽

Epithelial Mesenchymal Transition ◽

Luciferase Reporter ◽

Clinical Samples ◽

Expression Array ◽

Western Blot Assay ◽

Mesenchymal Transition ◽

Investigation Methods

Background/Aims: Pancreatic carcinoma (PC) is the one of the most common and malignant cancers worldwide. LncRNA taurine upregulated gene 1 (TUG1) was initially identified as a transcript upregulated by taurine, and the abnormal expression of TUG1 has been reported in many cancers. However, the biological role and molecular mechanism of TUG1 in PC still needs further investigation. Methods: Quantitative real-time PCR (qRT-PCR) was performed to measure the expression of TUG1 in PC cell lines and tissues. MTT and colony formation assays were used to measure the effect of TUG1 on cell proliferation. A wound healing assay, transwell assay and western blot assay were employed to determine the effect of TUG1 on cell migration and the epithelial mesenchymal transition (EMT) phenotype. RNA-binding protein immunoprecipitation (RIP) and a biotin-avidin pulldown system were performed to confirm the interaction between miR-328 and TUG1. A gene expression array analysis using clinical samples and RT-qPCR suggested that enhancer of zeste homolog 2 (EZH2) was a target of miR-382 in PC. Results: In this study, we reported that TUG1 was overexpressed in PC tissues and cell lines, and high expression of TUG1 predicted poor prognosis. Further experiments revealed that overexpressed TUG1 promoted cell proliferation, migration and contributed to EMT formation, whereas silenced TUG1 led to opposing results. Additionally, luciferase reporter assays, an RIP assay and an RNA-pulldown assay demonstrated that TUG1 could competitively sponge miR-382 and thereby regulate EZH2. Conclusion: Collectively, these findings revealed that TUG1 functions as an oncogenic lncRNA that promotes tumor progression, at least partially, by functioning as an endogenous ‘sponge’ and competing for miR-382 binding to the miRNA target EZH2.

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miR-491-3p is Downregulated in Retinoblastoma and Inhibit Tumor Cells Growth and Metastasis by Targeting SNN

Biochemical Genetics ◽

10.1007/s10528-020-10007-w ◽

2020 ◽

Author(s):

Yang Hu ◽

Ming Zhao ◽

Li Li ◽

Jie Ding ◽

Yu-Min Gui ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Lines ◽

Target Genes ◽

Expression Profiles ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Mesenchymal Transition ◽

Qrt Pcr ◽

Gene Assay ◽

E Cadherin

Abstract Retinoblastoma (Rb) is the most common pediatric malignant tumor of the eyes. Previous studies demonstrated that miR-491-3p is downregulated in various cancers. However, its function in Rb remains unknown. A total of 15 pairs of primary Rb tissues and adjacent noncancerous tissues were collected. Quantitative real-time PCR (qRT-PCR) was used to investigate the expression profiles of miR-491-3p. qRT-PCR, western blotting and in situ immunocytochemistry were performed to investigate the expression profiles of epithelial–mesenchymal transition-related proteins (E-cadherin, Vimentin and N-cadherin) in Rb tissues and Rb cell lines as well as cell morphology. Cell proliferation was estimated by MTS and colony formation assays. Apoptosis was determined by FACS, cell migration and invasion were analyzed using transwell chambers. MiR-491-3p’s target genes were predicted using target gene prediction databases. The interplay between miR-491-3p and SNN was evaluated through dual luciferase reporter gene assay. MiR-491-3p was significantly downregulated in mixed collection of 15 pairs of Rb tissues and Rb cell lines. Overexpression of miR-491-3p enhanced apoptosis, and significantly suppressed proliferation, migration and invasion of Rb cells. In contrast, the present of miR-491-3p inhibitor showed reversed results which apoptosis decreased, while cell proliferation of ARPE-19 cells increased. In addition, miR-491-3p increased the expression of E-cadherin, and dramatically decreased the expression of Vimentin and N-cadherin in Rb tissues and Rb cell lines, noticeable changes in morphology, too, as cells became less cohesive and more adhering. We found out that SNN was the pairing target of miR-491-3p and result showed that miR-491-3p and SNN interacted with each other. We also found out that the effects of miR-491-3p were in Rb cells were almost entirely canceled out at the overexpression of SNN. Our findings collectively suggest that miR-491-3p is an important tumor suppressor in Rb, which inhibits tumor growth and metastasis in Rb. These implicate it may be explored as a new therapeutic target in Rb.

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miR-18a-5p promotes NPC cell proliferation, invasion, migration, and EMT by targeting SMAD2

10.21203/rs.3.rs-36707/v2 ◽

2020 ◽

Author(s):

Pengcheng Li ◽

Junhui Xing ◽

Jianwu Jiang ◽

Xinyu Tian ◽

Xuemeng Liu ◽

...

Keyword(s):

Cell Proliferation ◽

Cell Lines ◽

Epithelial Mesenchymal Transition ◽

Luciferase Reporter Assay ◽

Luciferase Reporter ◽

Reporter Assay ◽

Mesenchymal Transition ◽

Metastasis Model ◽

Dual Luciferase Reporter Assay

Abstract Background Nasopharyngeal carcinoma (NPC) is the most common malignant tumor in the head and neck that is characterized by high local malignant invasion and distant metastasis. miR-18a-5p reportedly plays an important role in tumorigenesis and development. However, little is known about the mechanism underlying miR-18a-5p’s role in NPC. Methods Quantitative real-time PCR was used to detect the expression of miR-18a-5p in NPC tissues and cell lines. MTT assay and plate clone formation assay were used to detect the effect of miR-18a-5p on NPC cell proliferation. Wound healing assays and Transwell assays were used to detect the effect of miR-18a-5p on NPC cell invasion and migration. The expressions of epithelial mesenchymal transition (EMT)-related proteins N-cadherin, Vimentin, and E-cadherin were detected by Western blot. Bioinformatics and dual-luciferase reporter assay were used to detect the targeting interaction between miR-18a-5p and SMAD2. Xenotransplantation and metastasis model were used to detect the effect of miR-18a-5p on NPC growth and metastasis in vivo. Results miR-18a-5p was highly expressed in NPC tissues and cell lines. Overexpression of miR-18a-5p promoted NPC cell proliferation, invasion, migration, and EMT process, whereas inhibition of miR-18a-5p expression led to the opposite results. Results of dual-luciferase reporter assay showed that SMAD2 was the target gene of miR-18a-5p, and SMAD2 could reverse the effect of miR-18a-5p on NPC cell line. Xenotransplantation and metastasis model experiments in nude mice showed that miR-18a-5p promotes NPC growth and metastasis in vivo. Conclusions Targeting SMAD2 downregulated miR-18a-5p expression, thereby promoting NPC cell proliferation, invasion, migration, and EMT.

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MiRNA-206 suppresses PGE2-induced colorectal cancer cell proliferation, migration, and invasion by targetting TM4SF1

Bioscience Reports ◽

10.1042/bsr20180664 ◽

2018 ◽

Vol 38 (5) ◽

Cited By ~ 20

Author(s):

Young Ran Park ◽

Seung Young Seo ◽

Se Lim Kim ◽

Shi Mao Zhu ◽

Sungkun Chun ◽

...

Keyword(s):

Colorectal Cancer ◽

Cell Proliferation ◽

Cell Lines ◽

Epithelial Mesenchymal Transition ◽

Quantitative Polymerase Chain Reaction ◽

Luciferase Assay ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Control Group ◽

Mesenchymal Transition

MiRNA (miR)-206 plays a tumor suppressor role in various cancer types. Here, we investigated whether miR-206 is involved in prostaglandin E2 (PGE2)-induced epithelial–mesenchymal transition (EMT) in colorectal cancer (CRC) cells through the targetting of transmembrane 4 L six family member 1 (TM4SF1).The effect of PGE2 on growth and apoptosis of CRC cells was evaluated using the MTT assay and flow cytometry analysis, respectively. TM4SF1 and miR-206 expression levels were determined with quantitative polymerase chain reaction (qRT-PCR) in CRC tissues and cell lines. The concentration of PGE2 in the serum of CRC patients and healthy controls was measured with an ELISA kit. A miR-206 or TM4SF1 construct was transfected into cells with PGE2. Transwell migration and invasion assays were used to examine cell migration and invasion properties. Additionally, a luciferase assay was performed to determine whether TM4SF1 was directly targetted by miR-206.We found that miR-206 was down-regulated and TM4SF1 was up-regulated in human CRC tissues and cell lines. Moreover, miR-206 was negatively correlated with TM4SF1 expression. Bioinformatics analysis and a luciferase reporter assay revealed that miR-206 directly targetted the 3′-untranslated region (UTR) of TM4SF1, and TM4SF1 expression was reduced by miR-206 overexpression at both the mRNA and protein levels. Additionally, PGE2 significantly suppressed the expression of miR-206 and increased the expression of TM4SF1 in CRC cells. PGE2 induction led to enhanced CRC cell proliferation, migration, and invasion. Moreover, the overexpression of miR-206 decreased CRC cell proliferation, migration, and invasion compared with control group in PGE2-induced cells, and these effects could be recovered by the overexpression of TM4SF1. Overexpression of miR-206 also suppressed the expression of β-catenin, VEGF, MMP-9, Snail, and Vimentin and enhanced E-cadherin expression in PGE2-induced cells. These results could be reversed by the overexpression of TM4SF1. At last, up-regulation of miR-206 suppressed expression of p-AKT and p-ERK by targetting TM4SF1 in PGE2-induced cells.Our results provide further evidence that miR-206 has a protective effect on PGE2-induced colon carcinogenesis.

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